ArticleCellular and molecular life sciences : CMLS2022
Mfn2-mediated mitochondrial fusion promotes autophagy and suppresses ovarian cancer progression by reducing ROS through AMPK/mTOR/ERK signaling.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 129 citations in OpenAlex.
- Mdivi-1 augments chlorpromazine's anticancer effect via modulation of mitochondrial dynamics, hallmarks of cancer-related cellular behavior, and oxidative stress.Medical oncology (Northwood, London, England) · 2026Article
- AMPK-Mediated Lipid Metabolic Reprogramming in Cancer: From Mechanisms to Targeted Therapies.Cell biochemistry and function · 2026Review
- Subtype-specific mechanisms of lipid metabolism in gynecological malignancies and novel targeted intervention strategies (Review).Oncology letters · 2026Review
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- AGGF1 delays endothelial cellular senescence through the TGFB3-TAK1-AMPK signaling axis.Biogerontology · 2026Article
- The role of exercise in MFN2 regulation in osteoarthritis.Molecular biology reports · 2026Review
- Mitochondria-Associated Endoplasmic Reticulum Membranes in Cancer: Hubs for Tumor Progression and Therapeutic Vulnerabilities.Cell biology international · 2026Review
- Review
- Imbalances of mitochondrial dynamics in solid tumors.Oncogenesis · 2026Review
- Multiple machine learning algorithms construct cuproptosis genes and oxidative stress genes-related LncRNAs signature with prognostic and therapeutic relevance in ovarian cancer.Genes & genomics · 2026Article
- Caffeine Sodium Benzoate-Induced Macrophage M1 Polarization Promotes Endothelial Progenitor Cell Dysfunction by Inducing Mitochondrial Dysfunction Via Targeting let-7a-5p/OPA1 Axis.Applied biochemistry and biotechnology · 2026Article
- Mitofusin-2 suppresses tumor immune escape through EGFR/STAT3-mediated PD-L1 transcription.Cell death & disease · 2026Article
- Mfn1-mediated imbalanced mitochondrial dynamics promotes ovarian cancer stemness by inducing metabolic reprogramming.Journal of physiology and biochemistry · 2026Article
- Targeting Autophagy in Ovarian Cancer: The Emerging Role of Ginsenosides.Cancer medicine · 2026Review
- Autophagy in Cancer: Context-Dependent Regulation and Precision Nanomedicine-Enabled Therapeutic Targeting.Biomedicines · 2026Review
- Dynamin-Related Protein 1-Dependent Disruption of Mitochondrial Homeostasis Drives Blue Light-Induced Epithelial-Mesenchymal Transition in Retinal Aging.Aging cell · 2026Article
- Targeting mitochondrial homeostasis as a cancer treatment strategy: current status and future prospects.Molecular cancer · 2026Review
- Article
- ROS: their roles in diminished ovarian reserve.Frontiers in endocrinology · 2026Review
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dynamics are balanced fission and fusion events that regulate mitochondrial morphology, and alteration in these events results in mitochondrial dysfunction and contributes to many diseases, including tumorigenesis. Ovarian cancer (OC) cells exhibit fragmented mitochondria, but the mechanism by which mitochondrial dynamics regulators contribute to OC is considerably less clear. Here, we elucidated the potential role of Mfn2-mediated mitochondrial fusion in OC and present evidence that genetic or pharmacological activation of Mfn2 leads to mitochondrial fusion and reduces ROS generation, which correlates with reduced cell proliferation, invasion, migration, and EMT in OC cells. Also, increased mitochondrial fusion promotes the F-actin remodeling, reduces lamellipodia formation, and thus reduces EMT. Increased expression of Mfn2 triggers AMPK, promotes autophagy, reduces ROS, and suppresses OC progression by downregulating the p-mTOR (2481 and 2448) and p-ERK axis. OC patients with higher Mfn2 expression have better survival than those with lower Mfn2 levels. Our findings demonstrate that restoration of Mfn2-mediated mitochondrial fusion suppressed OC progression and suggest that this process could be a potential strategy in OC treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.